Early in 2007, Nowinski and Omalu heard that a coroner’s office in upstate New York might have some brain tissue from another former NFL player. Justin Strzelczyk, a Steelers offensive lineman like Webster and Long, was only thirty-six when he died in a fiery wreck after a high-speed police chase in 2004. In the six years since a knee injury ended his nine-season NFL career, Strzelczyk had spiraled into depression and paranoia. Friends and family no longer recognized the mountain of a man who looked like a grizzly but acted more like a teddy bear off the field. His behavior became erratic, his moods mercurial. He was sure his phone was tapped by the devil, and he complained of hearing voices from “the evil ones.” One morning, after his pickup truck brushed a car on the New York State Thruway while speeding at 100 mph, Strzelczyk caught the attention of some highway patrolmen, who gave chase. Forty miles later, when he failed to even slow down, the police threw spikes onto the road. With one tire blown out, he continued to fly down the highway, crossing over the median into oncoming traffic and, after another four harrowing miles, smashed into a tanker truck head-on. The autopsy showed no drugs or alcohol in his system. Strzelczyk’s friends and family were at a loss to explain what had happened to him.
Three years after the wreck, Nowinski called Strzelczyk’s mother and told her that he might be able to find some answers and give the family some closure. All he would need was her permission for Omalu to examine Strzelczyk’s brain for signs of CTE. Omalu received the brain early in the spring and began the process of slicing it up, sometimes moving his operation from his garage out to the balcony when the weather was warm and sunny. Once again, he sent the tissue samples out for staining and mounting. Once again, they came back with clear signs of CTE, this time verified by two independent neuropathologists. What was particularly striking about Strzelczyk’s case was that he was just in his mid-thirties and he had no reported concussions playing football at any level. That was the fourth case of CTE that Omalu had found out of the five brains he’d examined. The one brain with no abnormal proteins came from an active player who was just twenty-four when he died, which wasn’t surprising because CTE is a progressive disease that takes years to develop. Omalu began to lobby to have football-induced CTE recognized as a distinct condition. “Gridiron dementia,” he dubbed it.
Nowinski wasn’t limiting his investigations to football players. In the summer of 2007, when he read the shocking news that pro wrestler Chris Benoit had murdered his wife and his seven-year-old son before hanging himself, Nowinski wondered whether CTE had played any role in the tragedy. Nowinski knew Benoit from their WWE days and felt comfortable approaching the family to ask for the wrestler’s brain. When the stained slides came back, Omalu saw in a forty-year-old brain the worst case of CTE he’d observed up to that point. The findings made sense to Nowinski because Benoit had once admitted to having more concussions than he could count.
Benoit was the first athlete examined under the auspices of a newly formed organization called the Sports Legacy Institute. Nowinski, Omalu, Cantu, and another neurosurgeon, Dr. Julian Bailes, had founded the institute to formalize research into CTE. From the beginning, the group planned to affiliate with a major university. As it turned out, there was one right in Nowinski’s backyard. He learned of it fortuitously: one of his friends had been impressed with a presentation by a Boston University neuropsychologist, Robert Stern, on the link between head trauma and Alzheimer’s disease. The friend immediately called Nowinski suggesting he contact Stern, co-director of the Alzheimer’s Disease Clinical and Research Program at BU.
Stern and the Alzheimer’s program seemed to be exactly what Nowinski wanted for the Sports Legacy Institute. What made BU even more enticing was its connection with the Brain Bank at the Bedford VA Medical Center. Better still, the connection would offer a neuropathologist with decades of experience. Dr. Ann McKee had the kind of expertise that Nowinski was looking for. She was not only the neuropathologist for the Bedford VA, but she was also director for several brain banks housed there: the BU Alzheimer’s Disease Center, the Framingham Heart Study, and the Centenarian Study.
Not long afterward, the Sports Legacy Institute joined with the BU Alzheimer’s Disease Center to form the Center for the Study of Traumatic Encephalopathy. The new center would go a long way toward legitimizing research that had previously been in danger of being dismissed as sloppy and seat-of-the-pants. With her extensive experience examining both healthy and diseased brains, McKee would give the new center the credibility it needed.
• • •
Taped to the door of Ann McKee’s office is a broad black banner asking everyone who enters a whimsical question in white block letters: “got brains?”
The sign gives visitors their first sense of the scientist who works in the small, tightly packed office on the first floor of a nondescript brick building at the Bedford VA in eastern Massachusetts. Step inside and there are plenty of other clues to who she is. McKee’s desk is surrounded by curiosities that echo the whimsical note sounded on her door. Huddled atop one filing cabinet, Mr. Potato Head shares space with a skull and a bobblehead doll of New England Patriots quarterback Tom Brady. A statuette of another superstar quarterback, Brett Favre in his Green Bay Packers uniform, stands alongside medical texts on a bookshelf as a nod to the storied hometown franchise she’s rooted for since she was a little girl back in Wisconsin. A tomboy who grew up playing backyard football every summer, she would have followed her two older brothers onto the gridiron—“if,” she quips, “I hadn’t had the misfortune of being born a girl.”
The walls of the office are papered with photos of family and friends—and poster-sized images displaying the brains of people she’s become close to only after their deaths. Stacked in a small wooden filing cabinet beside McKee’s cluttered desk are sliding shelves containing stained slices from brains she’s already examined. McKee refers to each glass shelf by the name of the brain’s former owner—unless she’s been asked by family members not to divulge the identity of the person to whom the tissue belonged. In those cases, she simply refers to the shelf by some other identifying detail: the boxer, the football player, the eighteen-year-old.
She grabs one of the glass shelves and lays it on her desk to point out the differences between CTE and Alzheimer’s disease. Early on you can distinguish the two by their symptoms, she explains. Alzheimer’s patients exhibit memory problems right from the start. Those who suffer from CTE are more likely to demonstrate personality changes, like moodiness or anger. Late in the course of the two diseases, it can be impossible to tell them apart if you’re going only on symptoms. But when you look at the brains, the differences are unmistakable. Pointing to the brain tissue under glass, McKee says, “This was a man with Alzheimer’s disease. You can see how evenly distributed and regular the tau is.” The slice isn’t even magnified and still it’s impossible to miss the brownish tinge that signifies the presence of tau tangles in a multitude of neurons. Then she pulls out a second glass shelf and lays it next to the first one. “And this is a football player,” she says. “You can see how much more selective and patchy the tau deposits are.” What’s even more telling, she says, is that the brain of this football player, like many others with CTE, has no amyloid beta deposits. Though CTE sometimes comes with amyloid beta, the deposits are generally small.
Next, McKee points to a brain image from a boxer—her first case of CTE, back in 2003. She got the boxer’s brain shortly after he died. When the brain arrived, she didn’t know that it had come from a boxer, or even that he was old when he died. Whenever McKee first meets a new brain, she makes sure she has no background information on the person who originally owned it. She doesn’t want to know anything about the former owner’s death, or any diagnosed diseases. That kind of information would only serve to bias her first impression. She wants to make sure her judgments of this new acquaintance will be based solely on the brain tissue before her.
When she started to examine the boxer’s brain slices, she
was puzzled. She had never seen anything like this before: there was no amyloid beta, and the tau was distributed in an odd, patchy fashion. She could tell that this person had suffered from some sort of neurodegenerative disease, but she didn’t recognize which one it was. The one thing she did know for sure was that it wasn’t Alzheimer’s because there was no amyloid beta.
As the weeks passed, McKee continued to puzzle over the brain. She had her staff slice and prepare additional sections, but the more closely she examined the damage, the less it looked like anything she’d ever seen. There was one clue, though. Some of the slides suggested that the brain’s former owner had suffered from some sort of head trauma because the heaviest damage was in regions that are often harmed when the head is hit. But she couldn’t explain what that had to do with all the deterioration she was seeing. She pored through neuropathology texts, until one day she finally saw illustrations showing brain tissue from some ex-boxers. They looked so much like her guy that she was sure she was looking at someone who had been punch-drunk when he was alive.
As it turned out, the man had been living at the VA for years before his death at age seventy-two and his doctors had diagnosed him with Alzheimer’s disease. When McKee went to them with her findings, they told her that the man had been a professional boxer, a world champion in fact. They had assumed that the boxing had nothing to do with his dementia because he’d retired more than two decades before he started showing symptoms. They had assumed that if his dementia arose out of blows to the head while boxing, there would have been signs much sooner. McKee told the doctors what she had only recently learned herself: the neurodegenerative process that is kicked off by boxing usually doesn’t manifest itself with clear symptoms until many years after a fighter has quit the ring.
As far as the outside world was concerned, Paul Pender had died with Alzheimer’s disease. That’s what the obituaries all reported, quoting a Bedford VA spokeswoman who had gotten the diagnosis from his doctors. And that’s what the public perception would remain, since McKee and others have never revealed the identity of the CTE patient. Pender, a skinny Brookline firefighter-turned-prizefighter, was an unknown when he challenged Sugar Ray Robinson for the world middleweight championship in 1960. “Paul who?” the aging champ had deadpanned. Pender wrested the title from Robinson in a stunning upset, then proved that it wasn’t a fluke five months later by winning their rematch with another fifteen-round split decision. Pender went on to lose and regain the title over the next two years, then retired at age thirty-two after forty-eight pro bouts.
Eventually McKee put the intriguing case aside and didn’t think much about it until three years later, when another brain showed up with the same type of pathology. She quickly concluded that this was another boxer with CTE. Just as in the first case, the man had been living at the VA for years before he died. But when McKee went back to his doctors with her diagnosis, they told her that she must be wrong: the patient had no history of head trauma. They were convinced this was a case of Alzheimer’s, based on his symptoms. McKee was so sure her diagnosis was right that she called the man’s family to ask about his life and whether he’d had any history of head trauma. A little surprised, the family said that the man had indeed boxed in his twenties.
Two years later, when Chris Nowinski contacted her about examining brain tissue for the Center for the Study of Traumatic Encephalopathy, McKee was excited and enthusiastic. Here was a group offering to bring her more brains with possible CTE. She signed on right away. What made the partnership even more interesting to her was the promise of brains from athletes other than boxers. This was a chance to begin to answer questions about CTE, like how much head trauma it took to spark the development of the neurodegenerative disease.
The first of the football player brains arrived in fairly short order. It belonged to John Grimsley, a former Houston Oilers linebacker who had accidentally shot himself to death while cleaning a pistol early in 2008. During the years after his retirement, Grimsley had begun to show symptoms that worried his wife, Virginia. He had always been an easygoing guy, but now he was short-tempered and snappish. His memory problems were impossible to ignore. Over and over, she’d tell him something and it just wouldn’t stick in his brain. He’d go to the video rental store and bring back movies they’d just watched. On top of that, he was having regular headaches and problems sleeping. Virginia couldn’t figure out what was going on with her husband—until she saw a TV program that featured Chris Nowinski’s crusade to make football safer. The report included the stories of football players like Mike Webster and Terry Long, and their descent into dementia. Not long after that, John Grimsley shot himself. Virginia was sure the accident was the result of his deteriorating memory, that he had just forgotten there was a bullet in the chamber.
She was making arrangements for his funeral when the phone call came. A friend in the next room picked up and then called out to Virginia, “It’s someone named Chris Nowinski. He—”
Virginia interrupted and said, “Tell him I know who he is, and I know what he wants. Tell him he can have it.”
John Grimsley’s brain came to McKee from the coroner sliced and ready to be stained. Once she had the slides in front of her, McKee couldn’t help but be struck by how similar this brain looked to those of the boxers. Here again was the dark brown ribbon of tau tracing the outer rim of the brain. As with the boxers, there was so much tau that she could easily see the clumps with the naked eye. When she looked at the slices under the microscope, she could see that neurons had died in several regions of the brain, including the hippocampus—which might explain Grimsley’s problems with memory. She could also see dense patches of tau tangles scattered throughout a number of brain regions. Like the first boxer’s, this brain had not even a trace of amyloid beta. McKee was convinced: this was another case of CTE.
When asked how she knew that the pathology she was seeing in the forty-five-year-old football player was due to head trauma and not something that normally occurs in the general population, McKee had a ready answer. “I’ve looked at thousands of brains,” she said. “I have examined the brains of lots of eighty-year-olds from the Framingham study and it’s not normal to have this much tau. There are eighty-year-olds with nothing. In fact, I’ve examined the brain of a one-hundred-and-ten-year-old and it was pristine. I can tell you, this is not a normal part of aging.”
McKee wrote up a scholarly review of all known cases of CTE that had been confirmed by a neuropathologist and included her two boxers and the football player. The article was published in the Journal of Neuropathology & Experimental Neurology in July 2009. Meanwhile, athletes’ brains were showing up at a rate of one a month. By spring of 2010, McKee had examined the brains of twelve football players whose ages when they died ranged from eighteen to over eighty. All twelve had pathology consistent with CTE, varying from mild to severe. By this time McKee had also examined the brains of twelve other athletes in high-contact sports—boxers, wrestlers, and hockey players—and found CTE in all of them. Not all of the athletes had shown symptoms before they died. But in general, the more severe the pathology, the more likely it was that an athlete would have been showing clear signs of the disease.
McKee wasn’t the only neuropathologist busily autopsying athletes’ brains in search of CTE and other traumatically induced diseases. Bennet Omalu was also still on the trail of “gridiron dementia.” Following an acrimonious split with Nowinski, Omalu had teamed up with another disgruntled Sports Legacy Institute co-founder, the neurosurgeon Julian Bailes. The two doctors had become close after Bailes publicly defended Omalu’s groundbreaking postmortem studies in the face of the NFL’s harsh criticism. Bailes had a personal connection with the former players Omalu had autopsied, having gotten to know Mike Webster, Terry Long, and Justin Strzelczyk during a ten-year stint as a Steelers team physician. In 2009, Bailes launched his own CTE lab at West Virginia University, where he’d long served as chairman of neurosurgery, and tapped Omalu to help build
a brain bank similar to the one Nowinski and McKee ran. In short order, a heated rivalry sprang up between the two labs. They would compete for the brains of recently deceased players, once asking a family to split the brain 50-50 and sometimes publicly squabbling over which group deserved credit for a particular CTE diagnosis. Bailes and Omalu found themselves having to play catch-up with the well-oiled assembly line and publicity machine that Nowinski had built at BU with McKee and Cantu.
Nowinski, in the meantime, was innovating another strategy to build his brain bank: he had begun to solicit living players for brain donations. Instead of getting easier, it was getting harder to make cold calls to grieving relatives to ask for the brains of their just-deceased loved ones. He decided it would be a lot less daunting to ask the living to agree to donate their own brains upon death. By spring of 2010, he had commitments from more than three hundred athletes to donate their brains to his brain bank. “Some of the guys are doing it to protect their sons,” Nowinski says. “They recognize this is a problem, and they think if they can be part of the solution, they want to do it.” Included among athletes who agreed to donate their own brains is Nowinski himself. On the list of donation agreements gathered by Nowinski are some that had to be signed by wives rather than the athletes themselves. Though the players are still alive, they are too debilitated by dementia to make the decision. Among them are two former NFL teammates, John Mackey and Ralph Wenzel.
The Concussion Crisis Page 29
